OBJECTIVES: This study aims (i) to investigate the effects of EGCG on nadolol pharmacokinetics (maximum plasma concentration, time to achieve maximum concentration, area under the time-plasma concentration curve, plasma half-life and total clearance) and subsequently its impact on blood pressure control; and (ii) to identify transcriptional regulatory roles of EGCG on the nadolol intestinal and hepatic drug-transporters in SHR.
METHODS: Male SHR were pre-treated with a daily dose of EGCG (10 mg/kg body weight, i.g.) for 13 days. On day-14, a single dose of nadolol (10 mg/kg body weight) was given to the rats 30 min after the last dose of EGCG administration. Systolic blood pressure (SBP) was measured at 6-h and 22-h post-nadolol administration. Plasma and urinary nadolol concentrations were quantified using high-performance liquid chromatography, and pharmacokinetic parameters were analyzed by using non-compartmental analysis. Hepatic and ileal Oatp1a5, P-gp, and Oct1 mRNA expressions were determined by real-time PCR.
RESULTS: SBP of SHR pre-treated with EGCG and received nadolol was significantly higher than those which were not pre-treated with EGCG but received nadolol. Pre-treatment of EGCG resulted in a marked reduction of plasma nadolol maximum concentration (Cmax) and area under the time-plasma concentration curve (AUC) by 53% and 51% compared to its control. The 14-day treatment with oral EGCG led to a significant downregulation of mRNA levels of ileal Oatp1a5, P-gp, and Oct1 genes by 4.03-, 8.01- and 4.03-fold; and hepatic P-gp, and Oct1 genes by 2.61- and 2.66-fold.
CONCLUSION: These data concluded that exposure to EGCG could lead to reduced nadolol bioavailability and therefore, uncontrolled raised blood pressure and higher risks of cardiovascular events. Our data suggest that the reduced nadolol bioavailability is associated with the downregulation of ileal Oatp1a5 and Oct1 mRNA levels that subsequently lead to poor absorption of nadolol to the systemic circulation.
METHODS: A cross-sectional observational study of hospitalized COVID-19 patients was conducted. The neurological manifestations were divided into the self-reported central nervous system (CNS) symptoms, stroke associated symptoms, symptoms of encephalitis or encephalopathy and specific neurological complications. Multiple logistic regression was performed using demographic and clinical variables to determine the factors associated with outcome.
RESULTS: Of 156 hospitalized COVID-19 patients with mean age of 55.88 ± 6.11 (SD) years, 23.7% developed neurological complications, which included stroke, encephalitis and encephalopathy. Patients with neurological complications were more likely to have diabetes mellitus (p = 0.033), symptoms of stroke [limb weakness (p
METHODS: In this case-control study, we analyzed data on adult patients aged 18 years and above hospitalized for COVID-19 infection with matched hospitalized controls. The demographic, clinical data and anxiety measures using the Generalized Anxiety Disorder-7 questionnaire were analyzed using univariate and multivariate analysis.
RESULTS: 86.6% in the COVID-19 group had anxiety, significantly higher than 13.4% in the control group (p = 0.001). The COVID-19 group was significantly associated with the GAD-7 severity (p = 0.001). The number of COVID-19 patients in the mild, moderate, and severe anxiety groups was 48 (84.2%), 37 (86%), and 18 (94.7%), respectively. Multiple logistic regression showed significant predictors for anxiety, including COVID-19 diagnosis and neurological symptoms. Anxiety was found 36.92 times higher in the patients with COVID-19 compared to those without COVID-19 (OR 36.92;95% CI 17.09, 79.78, p = 0.001). Patients with neurological symptoms were at risk of having anxiety (OR 2.94; 95% CI 1.03, 8.41, p = 0.044).
DISCUSSION: COVID-19 patients experience a significant disruption in psychosocial functioning due to hospitalization. The burden of anxiety is notably high, compounded by a diagnosis of COVID-19 itself and neurological symptomatology. Early psychiatric referrals are warranted for patients at risk of developing anxiety symptoms.
METHODS: In the present cross-sectional study conducted at a tertiary teaching hospital, we aimed to investigate the prevalence and associated risk factors of undiagnosed depression in patients with epilepsy. We recruited patients with epilepsy aged 18-65 years after excluding those with background illnesses that may have contributed to the depressive symptoms. In total, 129 participants were recruited. We collected their demographic and clinical details before interviewing them using two questionnaires-the Neurological Disorders Depression Inventory for Epilepsy and Beck's Depression Inventory-II. Subsequently, if a participant screened positive for depression, the diagnosis was confirmed using the Diagnostic and Statistical Manual of Mental Disorders questionnaire, and a psychiatric clinic referral was offered.
RESULTS: Among the 129 participants, 9.3 % had undiagnosed major depressive disorder, and there was a female preponderance (66.7 %). The risk factors for undiagnosed depression among patients with epilepsy included low socioeconomic background (p = 0.026), generalized epilepsy (p = 0.036), and temporal lobe epilepsy (p = 0.010). Other variables such as being underweight and unmarried were more common among patients diagnosed with depression than without but no statistically significant relationship was found.
CONCLUSION: The prevalence of undiagnosed depression among patients with epilepsy was higher than that in population-based studies conducted in Western countries. Although questionnaires to screen for depression are widely available, some clinicians rarely use them and, therefore, fail to identify patients who may benefit from psychosocial support and treatment that would improve their disease outcomes and quality of life. The present study indicated that clinicians should use screening questionnaires to identify undiagnosed depression in people with epilepsy.